Reprezinta cresterea de volum a glandei tiroide, prin prezenta unor noduli, unici sau multipli, pastrand un nivel normal de hormoni tiroidieni.
Este un termen enspecific care defineste cresterea tiroidei in talie si in greutate de cause diverse, la persoanele eutiroidiene, hipotiroidiene sau hipertiroidiene. Etiopatogenie: 1. Defectul genetic de sinteza papillary thyroid cancer with vascular invasion hormone tiroidieni, apare in gusa congenitala- hormonii tiroidieni fiind insuficienti, hipofiza stimuleaza sinteza de hormone tropi, cee ace implica proliferarea epiteliului follicular tiroidian cu hiperplazia secundara a acestuia.
Goatrogenii varza si conopida si unele medicamenete, interfera cu productia de hormone tiroidieni si aparitia gusei. Gusa nodulara non toxica: este o crestere a tiroidei pe seama unei hiperplazii continute sau repretitive in raspunsul deficient de hormone secretati de glanda tiroida.
Clinic: Se observa masa cervicala ce comprima structurile din jur si determina simptome ca dispnee si disfagie; uneori poate fi prezent un nodul tiroidian hiperfunctional toxicsi se numeste sd. Plummer, iar clinic pacientul prezinta hipertiroidism. Tiroida poate fi crescuta in talie, sa ajunga pana la de grame. Se poate extinde substernal sis a determine detresa respiratorie.
Macroscopic: - gusa difuza: glanda marita uniform de volum mai mult de 40gsimetric, cu aspect cenusiu, translucid, sticlos din cauza prezentei coloidului; - gusa nodulara — marire de volum asimetrica, cu aspect multinodular pe sectiune; nodulii au aspect brun-galbui sau brun-roscat, papillary thyroid cancer with vascular invasion, in functie de cantitatea de coloid; nodulii sunt incapsulati; frecvent se observa zone hemoragice, chistice de scleroza si de calcificare.
Microscopic: Gusa difuza prezinta hiperplazie si hipertrofie difuza a epiteliului folicular, ocazional formand structuri papilare; pe masura ce afectiunea se cronicizeaza, cu episoade de stimulare si involutie administrare de iodaspectul coloid si nodular devind evident, cu foliculi dilatati chistic si epiteliu aplatizat sau cuboidal, nodulii au dimensiuni variabile si sunt separati prin septuri fibroase; frecvent se identifica zone de calcificare, scleroza, hemoragie si depozite de hemosiderina.
Two morphologic forms of goitre are distinguished: A. Diffuse goitre simple nontoxic goitre or colloid goitre. Nodular goitre multinodular goitre or adenomatous goitre.
Pathogenesis of Goitre The pathogenetic mechanisms of both forms of goitre can be considered together since nodular goitre is generally regarded as the end-stage of long-standing simple goitre Fig. The fundamental defect is deficient production of thyroid hormones due to various etiologic factors described below, but most common is dietary lack of iodine.
Sub Tiroida Sem 2
Deficient thyroid hormone production causes excessive TSH stimulation which leads to hyperplasia of follicular epithelium as well as formation of new thyroid follicles. Cyclical hyperplastic stage followed by involution stage completes the picture of simple goitre. Repeated and prolonged changes of hyperplasia result in continued growth of thyroid tissue while involuted areas undergo fibrosis, thus completing the picture of nodular goitre.
Diffuse Goitre Simple Non-toxic Goitre, Colloid Goitre Diffuse, nontoxic simple or colloid goitre is the name given to diffuse enlargement of the thyroid gland, papillary thyroid cancer with vascular invasion by hyperthyroidism.
Nicolau Institute of Virology, Bucharest, Romania. Introduction: In human cancer cells DNMTs are responsible for both de novo and maintenance methylation of tumor suppressor genes.
Most cases are in a state of euthyroid though they may have passed through preceding stage of hypothyroidism due to inadequate supply of iodine. TSH levels are invariably elevated. In general, goitre is more common in females. Simple goitre often appears at puberty or in adolescence, following which it may either regress or may progress to papillary thyroid cancer with vascular invasion goitre.
Epidemiologically, goitre occurs in 2 forms: endemic, and non-endemic or sporadic. Endemic goitre. Such endemic areas are several high mountainous regions far from the sea where iodine content of drinking water and food is low such as in the regions of the Himalayas, the Alps and the Ande.
Of late, however, the prevalence in these areas has declined due to prophylactic use of iodised salt.
Though most endemic goitres are caused by dietary lack of iodine, some cases occur due to goitrogens and genetic factors. Goitrogens are substances which interfere with the synthesis of thyroid hormones. These substances are drugs used in the treatment of hyperthyroidism and certain items of food such as cabbage, cauliflower, turnips and cassava roots.
Sporadic non- endemic goitre. Non-endemic or sporadic simple goitre is less common than the endemic variety. In most cases, the etiology of sporadic goitre is unknown. A number of causal influences have been attributed.
These include the following: Suboptimal iodine intake in conditions of increased demand as in puberty and pregnancy. Genetic factors. Dietary goitrogenes. Hereditary defect in thyroid hormone synthesis and transport dyshormonogenesis. Inborn errors of iodine metabolism.
Grossly, the enlargement of the thyroid gland in simple goitre is moderate weighing up to gmsymmetric and diffuse. Cut surface is gelatinous and translucent brown Fig.
Histologically, two stages are distinguished: 1. Hyperplastic stage is the early stage and is characterised by tall columnar follicular epithelium showing papillary infoldings and formation of small new follicles. Involution stage generally follows hyperplastic stage after variable period of time.
Papillomavirus sur gland stage is characterised by large follicles distended by colloid and lined by flattened follicular epithelium Fig. Nodular Goitre Multinodular Goitre, Adenomatous Goitre As already stated, nodular goitre is regarded as the end-stage of long-standing simple goitre.
It is characterised by most extreme degree of tumour-like enlargement of the thyroid gland and characteristic nodularity.
- DNMT1 expression in papillary thyroid carcinoma | ECE
- Sub Tiroida Sem 2
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The enlargement of the gland may be sufficient to not only cause cosmetic disfigurement, but in many cases may cause dsyphagia and choking due to compression of oesophagus and trachea. Since nodular goitre is derived from simple goitre, it has the same female preponderance but affects older individuals because it is a late complication of simple goitre.
Etiologic factors implicated in endemic and nonendemic or sporadic variety of simple goitre are involved in the etiology of nodular goitre too. However, how nodular pattern is produced is not clearly understood. Possibly, epithelial hyperplasia, generation of new follicles, and irregular accumulation of colloid in the follicles—all contribute to produce increased tension and stress in the thyroid gland causing rupture of follicles and vessels. This is followed by haemorrhages, scarring and sometimes calcification, resulting in development of nodular pattern.
Grossly, the thyroid in nodular goitre shows asymmetric and extreme enlargement, weighing gm or even more.
The five cardinal macroscopic features are as papillary thyroid cancer with vascular invasion Fig. Nodularity with poor encapsulation 2. Fibrous scarring 4. Focal calcification 5. Cystic degeneration. Cut surface generally shows multinodularity but occasionally there may be only one or two nodules which are poorly- circumscribed unlike complete encapsulation of thyroid adenoma, described below.
Histologically, the same heterogenicity as seen on gross appearance is seen. Corresponding microscopic features are as follows Fig. Partial or incomplete encapsulation of nodules.
The follicles varying from small to large and lined by flat to high epithelium. A few may show macropapillary formation. Areas of haemorrhages, haemosiderin-laden macrophages and cholesterol crystals. Fibrous scarring with foci of calcification. Micro-macrocystic change. Este cea mai frecventa cauza de hipertiroidism la persoanele sub 40 de ani, are incidenta maxima intre ani si un raport de in favoarea femeilor. Etiologie: factori genetici, mecanisme imune. Are porbabil, un mechanism immunologic si obisnuit este asosciata cu alte leziuni autoimmune.
Clinic: semnele hipertiroidismului: bolnavii afectati sunt femei tinere cu manifestari enrvoase, tahicardie, transpiratii, pierdere in greutate si exoftalmie. Nivelul tireotropinei este scazut sau inverted papilloma in the nose.